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nausea, vomiting, PO
decanoate Durabolin
:
Renal excretion:
q 3-4 wk peptic ulcer anticoagulants
Anabolic inj: 100, 200 unchanged
up-12 wk
diarrhea oxyphenbutazo
steroid mg/ml
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Oxandrolone Various; IM: 24 hr 6-8 days Liver metabolism: 2.5 mg bid-qid 0.1 mg/kg cholestatic anticoagulants
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Renal excretion:
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steroid for
an example:
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then
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intermittently
to maintain
weight
function tests
virilization
EPEC -O Self-Study Module 3b: Anorexia / Cachexia Page 21 of 52
EPEC -O Self-Study Module 3b: Anorexia/Cachexia 21 of 34
References
Module 3b: Anorexia / Cachexia
1 MacDonald N, Eason AM, Mazurak, et al. Understanding and managing
cancer cachexia. J Am Coll Surg. 2003;197:143-161; full text.
2 Cohn SH, Gartenhaus W, Sawitsky A, et al. Compartmental body composition
of cancer patients by measurement of total body nitrogen, potassium, and
water. Metabolism. 1981;30:222. PMID: 7207197.
In this study, the loss of body weight by patients with solid tumors consisted
primarily of the loss of muscle mass and body fat. Even in severe wasting,
patients appeared to retain significant amounts of body fat. Skeletal muscle
was predominantly lost; the visceral life-supporting system was, to a
considerable extent, spared. Nonmuscle tissue, including the visceral fraction,
did not change in this study, and actually appeared to increase in size when
comparison was made with the normal contrast population. The loss of total
body water was slight.
3 Dewys WD, Begg C, Lavin PT, et al. Prognostic effect of weight loss prior to
chemotherapy in cancer patients. Eastern Cooperative Oncology Group. Am J
Med. 1980;69:491-497. PMID: 7424938.
A multi-institutional study of 3,047 cancer patients from the Eastern
Cooperative Oncology Group is described. Loss of greater than 5% of
premorbid weight prior to chemotherapy predicted an early demise.
4 Staal-van den Brekel AJ, Shols AMW, ten Velde GPM, Buurman WA, Wouters
EFM. Analysis of the energy balance in lung cancer patients. Cancer Res.
1994;54:6430.
One hundred newly detected lung cancer patients were evaluated. Thirty
percent had a weight loss of 10% or more from their preillness stable weight.
An elevated resting energy expenditure was found in 74% of the patients.
Dietary intake was significantly lower in the weight-losing group.
EPEC -O Self-Study Module 3b: Anorexia/Cachexia 22 of 34
5 Stallings VA, Vaisman N, Chan HS, et al. Energy metabolism in children with
newly diagnosed acute lymphoblastic leukemia. Ped Res. 1989;26:154.
Nine patients (six females, three males) ages 6.5 to 15.8 y were studied. The
patients with a greater tumor burden had increased energy expenditure. Their
resting energy expenditure returned to normal in response to chemotherapy.
6 McGeer AJ, Detsky AS, O'Rourke K. Parenteral nutrition in cancer patients
undergoing chemotherapy: A meta-analysis. Nutrition1990;6:233.
Parenteral nutrition is not required for all patients undergoing intensive
cytotoxic therapy. Screening of nutritional status at the start of therapy and
monitoring oral intake following cytotoxic treatment may allow more
appropriate identification of patients requiring PN.
7 Anonymous. Parenteral nutrition in patients receiving cancer chemotherapy.
Ann Intern Med. 1989;110(9):734-736. PMID: 2494922; full text.
8 Slaviero KA, Clarke SJ, Rivory LP. Inflammatory response an unrecognized
source of variability in the pharmacokinetics and pharmacodynamics of cancer
chemotherapy. Lancet Oncol. 2003;4(4):224-233.
In this review, changes in the pharmacokinetics of medications caused by the
presence of inflammation are discussed.
9 Renton KW. Alteration of medication biotransformation and elimination during
infection and inflammation. Pharmacol Ther. 2001; 92(2-3):147-163; full text.
During infection or inflammation, the expression of cytochrome P450 and its
dependent biotransformation pathways are modified. This review covers the
loss that occurs in the major mammalian CYP families in response to
infection/inflammation and the mediator pathways that are key to this
response.
10 Loprinzi CL, Laurie JA, Wieand HS, et al. Prospective evaluation of prognostic
variables from patient-completed questionnaires. J Clin Oncol. 1994;12:601-
607.
In a North Central Cancer Treatment Group study of 1,115 patients with
colorectal and lung cancer, patients with a loss of appetite had a far poorer
prognosis compared with those who maintained their appetite, and this
observation persisted even after adjusting for several other prognostic
parameters.
EPEC -O Self-Study Module 3b: Anorexia/Cachexia 23 of 34
11 Balkwill F, Mantovani A. Inflammation and cancer: Back to Virchow? Lancet.
2001;357(9255):539-545; full text.
This article reviews the links between cancer and inflammation and discusses
the implications of these links for cancer prevention and treatment.
12 Khan S, Tisdale MJ. Catabolism of adipose tissue by a tumor-produced lipid-
mobilizing factor. Int J Cancer. 1999;80:444-447; full text.
Lipolysis in white adipose tissue during the process of cancer cachexia is
mediated by a tumor factor that stimulates cAMP production, possibly through
a beta-adrenergic receptor.
13 Cariuk P, Lorite MJ, Todorov PT, et al. Induction of cachexia in mice by a
product isolated from the urine of cachectic cancer patients. Br J Cancer.
1997;76(5):606-613.
Urine from cancer patients with weight loss showed the presence of an
antigen of M(r) 24,000. The antigen was not present in the urine of normal
subjects, patients with weight loss from conditions other than cancer, or
cancer patients who were weight-stable or with low weight loss (1 kg month(-
1)). The antigen is capable of producing a syndrome of cachexia in mice.
14 Hyltander A, Drott C, Korner U, et al. Elevated energy expenditure in cancer
patients with solid tumors. Br J Cancer. 1990;27(1):9-15.
Cancer patients (n=106) and noncancer subjects (n=96) were classified as
weight-stable (n=70) or weight-losing (n=132). Cancer patients had elevated
resting energy expenditure (REE) compared with either weight-losing (23.6
[0.4] vs. 20.5 [0.5] kcal/kg per day, P<0.001) or weight-stable controls (22.0
[0.6] vs. 17.9 [0.4], P<0.001). Increased metabolic rate was independent of
malnutrition and an elevated adrenergic state may be a likely explanation.
15 Simons JPF, Schols AMW, Buurman WA, Wouters EFM. Weight loss and low
body cell mass in males with lung cancer: Relationship with systemic
inflammation, acute phase response, resting energy expenditure, and
catabolic and anabolic hormones. Clin Sci. 1999;97:215-223; full text.
The article describes a study of 20 male lung cancer patients, prestratified by
weight loss of >10% (n=10) or <10% (n=10). Compared with the patients with
a weight loss of <10%, those with a weight loss of >10% were characterized
by higher levels of sTNF-R55 (trend towards significance; P=0.06), and lower
levels of albumin (27.4 compared with 34.4 mmol/l; P=0.02), testosterone
(13.2 compared with 21.5 nmol/l; P=0.01) and IGF-I (119 compared with 184
ng/ml; P=0.004).
EPEC -O Self-Study Module 3b: Anorexia/Cachexia 24 of 34
16 Laviano A, Meguid MM, Rossi-Fanelli Filippo. Cancer anorexia: Clinical
implications, pathogenesis, and therapeutic strategies. Lancet Oncol.
2003;4(11):686-694; full text.
The optimum therapeutic approach to anorectic cancer patients should include
changes in dietary habits, achieved via nutritional counseling and medication
therapy aimed at interfering with cytokine expression or hypothalamic
monoaminergic neurotransmission.
17 Torelli GF, Meguid MM, Moldawer LL, et al. Use of recombinant human
soluble TNF receptor in anorectic tumor-bearing rats. Am J Physiol.
1999;277(3 Pt 2);R850-855; full text.
Administration of anti-TNFa agent in tumor-bearing rodents resulted in an
improvement in weight and appetite compared with animals that received
vehicle only.
18 Baracos VE, DeVivo C, Hoyle DH, Goldberg AL. Activation of the ATP-
ubiquitin-proteasome pathway in skeletal muscle of cachectic rats bearing
hepatoma. Am J Physiol. 1995;268(5 Pt 1):E996-E1006.
The ubiquitin proteasome pathway accounts for >80% of lean tissue wasting in
cancer, as suggested by studies in an animal model.
19 Llovera M, Garcia-Martinez C, Lopez-Soriano J, et al. Role of TNF receptor 1
in protein turnover during cancer cachexia using gene knockout mice. Mol Cell
Endocrinol. 1998;142:183-189.
Implantation of Lewis lung carcinoma in gene knockout mice deficient in TNFa
demonstrated a different pattern of wasting compared with tumor-implanted
wild-type mice that manifested lower rates of protein degradation and less
activation of the ubiquitin proteasome system.
20 Llovera M, Garcia-Martinez C, Lopez-Soriano J, et al. Protein turnover in
skeletal muscle of tumor-bearing transgenic mice overexpressing the soluble
TNF receptor-1. Cancer Lett. 1998;130:19-27.
In this study, TNFa led to a doubling of expression of ubiquitin genes in
skeletal muscle.
EPEC -O Self-Study Module 3b: Anorexia/Cachexia 25 of 34
21 Todorov P, Cariuk P, McDevitt T, et al. Characterization of a cancer cachectic
factor. Nature. 1996;379:739; full text.
The authors discovered a 24-kilodalton proteoglycan from a tumor
homogenate from the MAC16 tumor line that produces cachexia in vivo by
inducing catabolism of skeletal muscle. The 24K material was also present in
urine of cachectic cancer patients, but was absent from normal subjects,
patients with weight loss due to trauma, and cancer patients with little or no
weight loss.
22 Todorov PT, McDevitt TM, Meyer DJ, Ueyama H, et al. Purification and
characterization of a tumor lipid-mobilizing factor. Cancer Res. 1998;58:2353.
Cancer patients with weight loss showed urinary excretion of a lipid-mobilizing
factor (LMF), determined by the ability to stimulate lipolysis in isolated murine
epididymal adipocytes. Such bioactivity was not detectable in the urine of
cancer patients without weight loss or in normal subjects.
23 Hirai K, Hussey HJ, Barber MD, Price SA, Tisdale MJ. Biological evaluation of
a lipid-mobilizing factor isolated from the urine of cancer patients. Cancer Res.
1998;58:2359.
In a study of 16 patients with cancer, only those with weight loss had
detectable concentrations of a lipid-mobilizing factor in their urine.
24 Woods D, Onambele G, Woledge R, et al. Angiotensin-I converting enzyme
genotype-dependent benefit from hormone replacement therapy in isometric
muscle strength and bone mineral density. J Clin Endocrinol Metab.
2001;86(5):2200-2204; full text.
In this study, subjects taking hormone replacement therapy showed a
significant gain in normalized muscle maximum voluntary force slope, the rate
of which was strongly influenced by ACE genotype.
25 Zigman JM, Elmquist JK. Minireview: From anorexia to obesity-the yin and
yang of body weight control. Endocrinology. 2003;144(9):3749-3756; full text.
In this review, the authors discuss the mechanisms by which metabolic signals
interact with key behavioral, neuroendocrine, and autonomic regulatory
regions of the central nervous system. They offer a model in which hormones
such as leptin and ghrelin interact with similar central nervous system circuits
and engage them in such a way as to maintain an appropriate and tight
regulation of body weight and food intake.
EPEC -O Self-Study Module 3b: Anorexia/Cachexia 26 of 34
26 Aleman MR, Santolaria F, Batista N. Leptin role in advanced lung cancer. A
mediator of the acute phase response or a marker of the status of nutrition?
Cytokine. 2002;19(1):21-26.; full text.
Seventy-six patients newly diagnosed with nonsurgical nonsmall-cell lung
cancer before chemotherapy treatment and 30 healthy controls were included
in this study. Body mass index, serum leptin and cholesterol levels, and
lymphocyte count were decreased in lung cancer patients. Cytokine IL-6, TNF-
alpha, sTNF-RII, sIL-2R, IL-12, IL-10, and IFN-gamma, and other acute phase
reactants such as alpha1 antitrypsin, ferritin, CRP, and platelets were all
raised in cancer patients, whereas IL-2 was decreased. Circulating leptin
concentrations were not elevated in weight-losing cancer patients and were
inversely related to the intensity of the inflammatory response.
27 Shimizu Y, Nagaya N, Isobe T, et al. Increased plasma ghrelin level in lung
cancer cachexia. Clin Cancer Res. 2003;9:774-778; full text.
Plasma ghrelin levels did not significantly differ between 43 patients with lung
cancer and controls (157 +/- 10 versus 132 +/- 8 fmol/ml, P = 0.1). However,
plasma ghrelin levels were significantly higher in patients with cachexia than in
those without cachexia (180 +/- 17 versus 135 +/- 10 fmol/ml, P = 0.011).
Increased ghrelin may represent a compensatory mechanism under catabolic-
anabolic imbalance.
28 Slaviero KA, Clarke SJ, Rivory LP. Inflammatory response: An unrecognized
source of variability in the pharmacokinetics and pharmacodynamics of cancer
chemotherapy. Lancet Oncol. 2003;4(4):224-233.
29 Chang VT, Hwang SS, Feuerman M. Validation of the Edmonton Symptom
Assessment Scale. Cancer. 2000;88(9):2164-2171.
30 European Organisation for Research and Treatment of Cancer. EORTC
quality of life questionnaire (QLQ C-30). Available at:
http://www.eortc.be/home/qol/ExplQLQ-C30.htm. Accessed March 26, 2005.
31 Kaasa T, Loomis J, Gillis K, Bruera E, Hanson J. The Edmonton Functional
Assessment Tool: Preliminary development and evaluation for use in palliative
care. J Pain Symptom Manage. 1997;13(1):10-19.
32 American College of Physicians. Parenteral nutrition in patients receiving
cancer chemotherapy. Ann Intern Med. 1989;110(9):734-736.
This is a commentary on the use of parenteral nutrition in patients with cancer.
EPEC -O Self-Study Module 3b: Anorexia/Cachexia 27 of 34
33 Ovesen L, Allingstrup L, Hannibal J, Mortenson EL, Hansen OP. Effect of
dietary counseling on food intake, body weight, response rate, survival, and
quality of life in cancer patients undergoing chemotherapy: A prospective,
randomized study. J Clin Oncol. 1993;11:2043-2049.
In this study, 105 cancer patients who were receiving chemotherapy were
randomly assigned to nutritional counseling versus no such counseling.
Patients who received counseling ate more, but this increased caloric intake
led to no significant weight gain, no significant improvement in quality of life,
no improvement in tumor response rate to chemotherapy, and no survival
advantage within the group that received counseling.
34 Loprinzi CL, Kugler JW, Sloan JA, et al. Randomized comparison of megestrol
acetate versus dexamethasone versus fluoxymesterone for the treatment of
cancer anorexia/cachexia. J Clin Oncol. 1999;17:3299-3306; full text.
In this study, fluoxymesterone resulted in significantly less appetite
enhancement and did not have a favorable toxicity profile. Megestrol acetate
and dexamethasone caused a similar degree of appetite enhancement and
similar changes in nonfluid weight status, with nonsignificant trends favoring
megestrol acetate for both of these parameters. Dexamethasone was
observed to have more corticosteroid-type toxicity and a higher rate of
medication discontinuation because of toxicity and/or patient refusal than
megestrol acetate (36% v 25%; P =.03).
35 Loprinzi CL, Ellison NM, Schaid DJ, et al. Controlled trial of megestrol acetate
for the treatment of cancer anorexia and cachexia. J NCI. 1990;82:1127-1132.
One hundred thirty-three cancer patients with the cancer anorexia/weight loss
syndrome participated in a North Central Cancer Treatment Group trial.
Patients who received megestrol acetate at a dose of 800 mg/day reported an
improved appetite and an increase in nonfluid weight.
36 Moertel CG, Schutt AJ, Reitemeier RJ, Hahn RG. Corticosteroid therapy of
preterminal gastrointestinal cancer. Cancer. 1974;33:1607-1609. PMID:
4135151.
37 Loprinzi CL, Bernath AM, Schaid DJ, et al. Phase III evaluation of 4 doses of
megestrol acetate as therapy for patients with cancer anorexia and/or
cachexia. J Clin Oncol. 1993;11:762-767.
The authors report finding through a direct dose-response endpoint that
megestrol acetate given in doses of 480 to 800 mg/day was more effective
than a dose of 160 mg/day. The higher dose of 1,280 mg/day was not any
more effective.
EPEC -O Self-Study Module 3b: Anorexia/Cachexia 28 of 34
38 Personal communication.
39 Lambert CP, Sullivan DH, Freeling SA, et al. Effects of testosterone
replacement and/or resistance exercise on the composition of megestrol
acetate stimulated weight gain in elderly men: A randomized controlled trial. J
Clin Endocrinol Metab. 2002;87(5):2100-2106; full text.
Thirty older men (aged 67.0 +/- 5.8) completed this 12-week study. All subjects
received megestrol acetate and were randomly assigned to a treatment group.
The mean increase in body weight for all groups did not differ between groups.
Despite significant weight gain, megestrol acetate appears to have an
antianabolic effect on muscle size even when combined with testosterone
replacement. Resistance exercise attenuated this reduction in muscle mass
and when combined with testosterone had an anabolic effect on muscle mass.
40 Loprinzi CL, Fonseca R, Jensen MD. Megestrol acetate-induced adrenal
suppression [letter]. J Clin Oncol. 1996;14:689. PMID: 8636799.
41 Harrold JA, Williams G. The cannabinoid system: A role in both the
homeostatic and hedonic control of eating? Br J Nutr. 2003;90:729-734; full
text.
The authors report that cannabinoid system activity in the hypothalamus is
thought to contribute to the homeostatic regulation of energy balance, under
the control of the hormone leptin. A second component of cannabinoid-
mediated food intake appears to involve reward pathways and the hedonic
aspect of eating.
42 Sakamoto M, Mikasa K, Toshimasa M, et al. Anti-cachectic effect of
clarithromycin for patients with unresectable non-small cell lung cancer.
Chemotherapy. 2001;47:444-451; full text.
Clarithromycin was administered to 33 patients with unresectable primary
nonsmall-cell lung cancer who had received chemotherapy, radiotherapy, or
both (basic cancer therapy). After 3 months of clarithromycin treatment, serum
levels of IL-6 significantly decreased and body weight increased.
43 Von Roenn JH, Tchekmedyian S, Hoffman R, et al. Safety of oxandrolone in
cancer-related weight loss. ASCO Poster #3013. 2003.
44 Calder PC. More good news about fish oil. Nutrition. 2001;17:158-160. full
text.
45 Tisdale MJ. Protein loss in cancer cachexia. Science. 2000;289:2293-2294.
PMID: 11041796; full text.
EPEC -O Self-Study Module 3b: Anorexia/Cachexia 29 of 34
46 Hardman WE, Moyer MP, Cameron IL. Consumption of an omega-3 fatty acid
product, INCELL AAFA reduced side-effects of CPT-11 (ironotecan) in mice.
Br J Cancer. 2002;86:983-988; full text.
In this study, a 2% omega-3 polyunsaturated fatty acid product containing a
high concentration of long-chain fatty acids in the diet reduced the side effects
of CPT-11 treatment in mice.
47 Gogos CA, Ginopoulos P, Salsa B, et al. Dietary omega-3 polyunsaturated
fatty acids plus vitamin E restore immunodeficiency and prolong survival for
severely ill patients with generalized malignancy: A randomized control trial.
Cancer. 1998;82:395-402; full text.
Sixty patients with generalized solid tumors were randomized to receive
dietary supplementation with either fish oil (18 g of omega-3 polyunsaturated
fatty acids, PUFA) or placebo daily until death. Each group included 15 well-
nourished and 15 malnourished patients. Omega-3 polyunsaturated fatty acids
had a significant immunomodulating effect and seemed to prolong the survival
of malnourished patients with generalized malignancy.
48 Jatoi A, Rowland KH Jr, Loprinzi Cl, et al. A Phase III, double blind, placebo
controlled randomized comparison of megestrol acetate (megace) versus an
omega-3 fatty acid (EPA-enriched nutritional supplement versus both).
Abstract. American Society of Clinical Oncology; 2003.
49 Fearon KCH, von Meyenfeldt MF, Moses AGW, et al. Effect of a protein and
energy dense n-3 fatty acid enriched oral supplement on loss of weight and
lean tissue in cancer cachexia: A randomised double blind trial. Gut.
2003;52:1479-1486; full text.
Two hundred patients were randomized to consume two cans/day of the
experimental (n-3 fatty acids, especially eicosapentaenoic acid) or control
supplement for 8 weeks in a multicenter, randomized, double-blind trial.
Patients in both groups stopped losing weight. Group comparisons indicated
that at the mean dose taken, enrichment with n-3 fatty acids did not provide a
therapeutic advantage.
EPEC -O Self-Study Module 3b: Anorexia/Cachexia 30 of 34
50 Clark RH, Feleke G, Mehraj D, et al. Nutritional treatment for acquired
immunodeficiency virus-associated wasting using b-hydroxy b-methylbutyrate,
glutamine, and arginine: A randomized, double-blind, placebo-controlled study.
JPEN J Parenter Enteral Nutr. 2000;24(3):133-139.
Sixty-eight human immunodeficiency virus (HIV)-infected patients with a
documented weight loss of at least 5% in the previous 3 months were
randomly assigned in a double-blind fashion to receive either placebo
containing maltodextrin or a nutrient mixture containing 3 g HMB, 14 g L-
glutamine, and 14 g L-arginine given in 2 divided doses daily for 8 weeks.
Forty-three subjects completed the 8-week protocol, (placebo, n=21;
HMB/Arg/Gln, n=22). At 8 weeks, subjects consuming the HMB/Arg/Gln
mixture gained 3.0 +/- 0.5 kg of BW while those supplemented with the
placebo gained 0.37 +/- 0.84 kg (p=.009).
51 Ross JA, Fearon KCH. Eicosanoid-dependent cancer cachexia and wasting.
Curr Opin Clin Nutr Metab Care. 2002;5(3):241-248; full text.
This review examines the biology of the eicosanoids and the evidence of a
role for the eicosanoids in cancer cachexia and wasting.
52 Lonroth C, Svaninger G, Gelin J, et al. Effects related to indomethacin
prolonged survival and decreased tumor growth in a mouse tumor model with
cytokine dependent cancer cachexia. Int J Oncol. 1995;7:1405-1413.
53 Wigmore SJ, Barber MD, Ross JA, et al. Effect of oral eicosapentaenoic acid
on weight loss inpatients with pancreatic cancer. Nutr Cancer. 2000;36:177-
184.
Twenty-six patients with advanced pancreatic cancer were entered into the
study. Eicosapentanenoic acid (95% pure) was administered at 1 g/day; the
dose was increased to 6 g/day over 4 weeks, and a maintenance dose of 6
g/day was then administered. After 4 weeks of supplementation, patients had
a median weight gain of 0.5 kg (p=0.0009 vs. rate of weight loss at baseline),
and this stabilization of weight persisted over the 12-week study period.
54 McMillan DC, Wigmore SJ, Fearon KCH, et al. A prospective randomized
study of megestrol acetate and ibuprofen in gastrointestinal cancer patients
with weight loss. Br J Cancer. 1999;79:495-500; full text.
In this study, 38 and 35 patients (median weight loss 18%) were randomized
to megestrol acetate/placebo or megestrol acetate/ibuprofen, respectively, for
12 weeks. Forty-six (63%) of the patients failed to complete the 12-week
assessment. Of those evaluable at 12 weeks, there was a decrease in weight
(median 2.8 kg) in the megestrol acetate/placebo group compared with an
increase (median 2.3 kg) in the megestrol acetate/ibuprofen group (P<0.001).
EPEC -O Self-Study Module 3b: Anorexia/Cachexia 31 of 34
55 Davis TW, Zweifel BS, O'Neal JM, et al. Inhibition of cyclooxygenase-2 by
celexicob reverses tumor-induced wasting. J Pharmacol Exp Ther.
2004;308(3):929-934; full text.
The authors report that despite the observation that no significant impact on
tumor growth was observed between vehicle and celecoxib-treated animals
over the course of the mouse studies, celecoxib rapidly reversed weight loss.
56 Lunholm K, Daneryd P, Korner U, et al. Evidence that long term COX-
treatment improves energy homeostasis and body composition in cancer
patients with progressive cachexia. Int J Oncol. 2004;24:505-512.
A retrospective case control analysis was performed. Weight-losing, untreated
cancer patients had elevated resting energy expenditure compared with
undernourished noncancer patients (23.3+-/-0.1,m=702 vs. 20.9+/-0.3
kcal/kg/day, n=132, P<0.001). This difference was significantly reduced by
long-term indomethacin treatment (P<0.003).
57 Girodin F, Galan P, Monget AL, et al. Impact of trace elements and vitamin
supplementation on immunity and infections in institutionalized elderly
patients. Arch Intern Med. 1999;159:748-754; full text.
This randomized, double-blind, placebo-controlled intervention study included
725 institutionalized elderly patients (>65 years) from 25 geriatric centers in
France. Patients received an oral daily supplement of nutritional doses of trace
elements (zinc and selenium sulfide) or vitamins (beta carotene, ascorbic acid,
and vitamin E) or a placebo within a 2 x 2 factorial design for 2 years. The
number of patients with respiratory tract infections during the study was lower
in groups that received trace elements (P=.06).
58 Fairfield KM, Fletcher RH. Vitamins for chronic disease prevention. JAMA.
2002;287(23):3117-3125; full text.
Some groups of patients are at higher risk for vitamin deficiency and
suboptimal vitamin status. Inadequate intake of several vitamins has been
linked to chronic diseases, including coronary heart disease, cancer, and
osteoporosis.
EPEC -O Self-Study Module 3b: Anorexia/Cachexia 32 of 34
59 Mantovani G, Maccio A, Madeddu C, et al. Antioxidant agents are effective in
inducing lymphocyte progression through cell cycle in advanced cancer
patients: Assessment of the most important laboratory indexes of cachexia
and oxidative stress. J Mol Med. 2003;81(10):664-673; full text.
In this study the percentage of phytohemaglutinin-stimulated peripheral blood
mononuclear leukocytes of cancer patients entering S phase, which was
significantly lower than that of controls, increased significantly to greater than
physiological levels after coculture with antioxidants. Serum levels of IL-1 beta,
IL-6, and TNFalpha were significantly higher and serum levels of IL-2 and
leptin were significantly lower in cancer patients than controls. Serum levels of
C-reactive protein and fibrinogen were significantly higher in cancer patients
than controls. Patients with advanced cancer thus exhibited both a high-grade
oxidative stress and a chronic inflammatory condition.
60 Thune I, Brenn T, Lund E, et al. Physical activity and the risk of breast cancer.
N Engl J Med. 1997;336:1269-1275; full text.
During a median follow-up of 13.7 years, the authors identified 351 cases of
invasive breast cancer among the 25,624 women in the cohort. Greater
leisure-time activity was associated with a reduced risk of breast cancer.
(Relative risk, 0.63; 95% confidence interval, 0.42 to 0.95) among women who
exercised regularly, as compared with sedentary women (P for trend=0.04.)
61 Segal RJ, Reid RD, Courneya KS. Resistance exercise in men receiving
androgen deprivation therapy for prostate cancer. J Clin Oncol.
2003;21(9):1651-1652; full text.
Men assigned to resistance exercise had less interference from fatigue on
activities of daily living (P=.002) and higher quality of life (P =.001) than men in
the control group.
62 Galvao DA, Newton RU. Review of exercise intervention studies in cancer
patients. J Clin Oncol. 2005;23:899-909.
Twenty-six studies were reviewed. The majority demonstrated physiological
and psychological benefits. Most studies involved breast cancer patients.
Recent evidence supports resistance exercise (e.g., weight training) over
cardiovascular exercise (e.g., walking) to counteract some side effects of
cancer management and improve physical function and quality of life.
EPEC -O Self-Study Module 3b: Anorexia/Cachexia 33 of 34
63 Courneya KS, Mackey JR, Bell GJ, et al. Randomized controlled trial of
exercise training in postmenopausal breast cancer survivors: Cardiopulmonary
and quality of life outcomes. J Clin Oncol. 2003;21(9):1651-1652; full text.
Fifty-two participants completed the trial. Overall quality of life increased by 9.1
points in the exercise group compared with 0.3 points in the control group
(mean difference, 8.8 points; 95% CI, 3.6 to 14.0; P=.001).
64 Lucia A, Earnest C, Perez M. Cancer-related fatigue: Can exercise physiology
assist oncologists? Lancet Oncol. 2003;4(10):616-625; full text.
The authors report that advising fatigued cancer patients to rest paradoxically
compounds symptoms of fatigue, since sedentary habits induce muscle
catabolism and thus cause a further decrease in functional capacity. By
contrast, there is scientific evidence that an exercise program of low to
moderate intensity can substantially reduce cancer-related fatigue and
improve the quality of life of these patients.
65 Binder EF, Schechtman KB, Ehsani AA, et al. Effects of exercise training on
frailty in community-dwelling older adults: Results of a randomized, controlled
trial. JAGS. 2002;50:1921-1928.
In 115 sedentary men and women (mean age 83) with mild to moderate
physical frailty, exercise therapy resulted in significantly greater improvements
than home exercise (control).
EPEC -O Self-Study Module 3b: Anorexia/Cachexia 34 of 34